Heart failure (HF) is a debilitating disease in which abnormal function of the heart leads in the direction of inadequate blood flow to fulfill the needs of the tissues and organs of the body. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately eject or fill with blood between heartbeats and the valves regulating blood flow become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness and the inability to carry out daily tasks may result. Not all HF patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As HF progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it can add muscle causing the ventricles (particularly the left ventricle) to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output, resulting in elevated pressures within the left atrium. Elevated left atrial pressure (LAP) can then exacerbate the HF, particularly congestive HF where the weak pumping of the heart leads to a build-up of fluids in the lungs and other organs and tissues. Often, a progression of HF and the build-up of congestive fluids results in the patient being hospitalized.
Despite current therapies, the rate of HF hospitalizations remain high—about 1.1 million HF hospitalizations annually. A new approach to managing patients has exploited chronic measurements of pulmonary arterial pressures. Pulmonary artery pressure (PAP) is generated by the right ventricle (RV) ejecting blood into the pulmonary circulation, which acts as a resistance to the output from the RV. With each ejection of blood during ventricular systole, pulmonary arterial blood volume increases which stretches the wall of the artery. As the heart relaxes, blood continues to flow from the pulmonary artery into the pulmonary circulation. The smaller arteries and arterioles serve as the chief resistance vessels, and through changes in their diameter, regulate pulmonary vascular resistance. In the recent CHAMPION study, the use of a wireless implantable PAP sensor showed a 30% percent reduction in HF hospitalizations in six months in New York Heart Association (NYHA) Class III HF patients in a prospective, multi-center, randomized (1:1) controlled single blinded clinical trial (n=553). (See, Abraham et al., “Wireless pulmonary artery haemodynamic monitoring in chronic heart failure: a randomised controlled trial,” Lancet 2011; 377:658-666.) Use of daily PAP measurements allowed physicians to proactively monitor and tailor the patient's pharmacological therapy. Note that the CHAMPION study was directed to the use of a PAP sensor provided by CardioMEMS, Inc., which operates in conjunction with an external PAP monitor. Briefly, the PAP sensor is implanted within the pulmonary artery of the patient using a catheter. Thereafter, once per day (or at some other periodic interval), the patient places an interface device over his or her chest, which receives PAP data wirelessly from the implanted sensor for routing to a clinician for review.
Although PAP monitors of the type used in the CHAMPION study are quite useful, such systems currently provide no atrial pulsatile hemodynamic data, which would be helpful to the clinician. Moreover, in circumstances where atrial fibrillation (AF) induces an increase in LAP within the patient (thereby also increasing end diastolic PAP), there appears to be no current method to distinguish this condition from increases in LAP associated with HF progression. Accordingly, it would be desirable to provide PAP-based techniques for distinguishing changes in PAP due to AF or other arrhythmias from changes due to progression of HF. This would allow the clinician to more effectively establish an appropriate treatment plan (e.g. to determine whether pharmacological adjustments are warranted or AF ablations should be performed.)
In this regard, note that AF is the most common arrhythmia. According to the Framingham Heart Study, AF has a prevalence of about 4% in the adult population. (See, Kannel et al, “Epidemiologic features of chronic atrial fibrillation: The Framingham Study,” NEJM. 1982; 306:1018-22.) As the patient population continues to age, the prevalence of AF rises as well, from less than 0.05 percent in patients 25 to 35 years of age to more than 5% patients over 69 years of age. (See, Furberg et al., “Prevalence of atrial fibrillation in elderly subjects (The Cardiovascular Health Study),” Am J Cardiol. 1994; 74:236-241.) In the HF patient population, AF, premature ventricular contractions (PVCs) and ventricular arrhythmias are a common co-morbidity. In the Framingham Heart Study, 1470 participants developed either HF or a new AF between the years 1948 and 1995. Moreover, the prevalence of AF in patients with HF increased in parallel with the severity of the disease, ranging from 5% in patients with mild HF to 10% to 26% among patients with moderate HF and up to 50% in patients with severe HF.